Glaucoma is a blinding disease characterized by progressive degeneration of retinal ganglion cell and loss of visual function. While elevation of intraocular pressure (IOP) is a major risk factor for development and progression of glaucoma, the exact molecular and cellular mechanisms of glaucoma remain obscure1. All the available treatment options currently available for glaucoma patients aim to lower the IOP. Understanding the mechanisms and devising new treatment strategies to prevent blindness are unmet needs in glaucoma management.
Inducing IOP elevation in animal models is an important strategy for investigation of the mechanisms of retinal ganglion cell degeneration, and development and testing of new drugs and neuroprotective therapies for glaucoma. A number of experimental glaucoma models have been described in the literature. These include the transgenic DBA/2J mouse model2-4, cauterization of episcleral vein5-17, injection of hyertonic saline18-22, laser photocoagulation of the trabecular meshwork23-31, and intracameral injection of microbeads32-38 and/or hyaluronic acid39-40. Although these models afford IOP elevation resulting in retinal ganglion cell degeneration, the longitudinal profile of IOP elevation in these models does not recapitulate to what researchers observe in glaucoma patients. Specifically, the IOP elevation is often transient, with high IOP spikes after induction of IOP elevation. Another side effect commonly encountered is development of cataract and corneal opacities, which would obscure in vivo examination of the optic nerve and retina. An ideal glaucoma model should demonstrate chronic (in terms of months, not weeks) and moderate elevation of IOP (high IOP elevation may result in retinal ischemia), with a clear optical media. Since these attributes are absent in the currently available glaucoma models, there exists a distinct need for developing new and better animal models for glaucoma research. The present invention fulfills this and other related needs.